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首页> 外文期刊>Applied Microbiology >Global Transcriptome and Mutagenic Analyses of the Acid Tolerance Response of Salmonella enterica Serovar Typhimurium
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Global Transcriptome and Mutagenic Analyses of the Acid Tolerance Response of Salmonella enterica Serovar Typhimurium

机译：肠道沙门氏菌鼠伤寒沙门氏菌的耐酸反应的全球转录组和诱变分析。

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Salmonella enterica serovar Typhimurium ( S . Typhimurium) is one of the leading causative agents of food-borne bacterial gastroenteritis. Swift invasion through the intestinal tract and successful establishment in systemic organs are associated with the adaptability of S . Typhimurium to different stress environments. Low-pH stress serves as one of the first lines of defense in mammalian hosts, which S . Typhimurium must efficiently overcome to establish an infection. Therefore, a better understanding of the molecular mechanisms underlying the adaptability of S . Typhimurium to acid stress is highly relevant. In this study, we have performed a transcriptome analysis of S . Typhimurium under the acid tolerance response (ATR) and found a large number of genes (～47%) to be differentially expressed (more than 1.5-fold or less than ?1.5-fold; P < 0.01). Functional annotation revealed differentially expressed genes to be associated with regulation, metabolism, transport and binding, pathogenesis, and motility. Additionally, our knockout analysis of a subset of differentially regulated genes facilitated the identification of proteins that contribute to S . Typhimurium ATR and virulence. Mutants lacking genes encoding the K~(+) binding and transport protein KdpA, hypothetical protein YciG, the flagellar hook cap protein FlgD, and the nitrate reductase subunit NarZ were significantly deficient in their ATRs and displayed varied in vitro virulence characteristics. This study offers greater insight into the transcriptome changes of S . Typhimurium under the ATR and provides a framework for further research on the subject.
机译：肠炎沙门氏菌鼠伤寒沙门氏菌（S. Typhimurium）是食源性细菌性肠胃炎的主要病原体之一。 S的适应性与肠道的迅速入侵和在系统器官中的成功建立有关。鼠伤寒能适应不同的压力环境。低pH胁迫是哺乳动物宿主S的第一道防线之一。鼠伤寒必须有效克服以建立感染。因此，更好地理解了S适应性的分子机制。鼠伤寒与酸胁迫高度相关。在这项研究中，我们进行了S的转录组分析。鼠伤寒在酸耐受反应（ATR）下，发现大量基因（〜47％）被差异表达（大于1.5倍或小于？1.5倍; P <0.01）。功能注释显示差异表达的基因与调节，代谢，转运和结合，发病机理和运动性有关。此外，我们对差异调节基因子集的敲除分析有助于鉴定有助于S的蛋白质。鼠伤寒ATR和毒力。缺少编码K〜（+）结合和转运蛋白KdpA，假设蛋白YciG，鞭毛钩帽蛋白FlgD和硝酸还原酶亚基NarZ的基因的突变体的ATR明显不足，并显示出多种体外毒力特征。这项研究提供了更深入的了解S的转录组变化。 ATR下的鼠伤寒提供了进一步研究的框架。

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